Cardiac Muscle Physiology

Action Potentials in Cardiac Muscle Cells

Cardiac muscle cells (cardiomyocytes) generate action potentials that differ significantly from those in skeletal muscle. These differences are crucial for the heart's function as a rhythmic pump.

• Resting Membrane Potential: Cardiac myocytes have a resting potential of approximately -90 mV, which is more negative than that of skeletal muscle cells.

• Depolarization: Initiated by voltage-gated sodium (Na+) channels, causing a rapid influx of Na+ and a sharp rise in membrane potential.

• Initial Repolarization: Fast-opening potassium (K+) channels briefly open, causing a small drop in potential.

• Plateau Phase: Voltage-gated L-type calcium (Ca2+) channels open, allowing Ca2+ influx, which maintains depolarization and creates a plateau. This phase is unique to cardiac muscle and is absent in skeletal muscle.

• Final Repolarization: Ca2+ channels close, and slow-opening K+ channels open, returning the cell to resting potential.

• No Hyperpolarization: Unlike neurons and skeletal muscle, cardiac myocytes do not exhibit an undershoot or hyperpolarization phase.

Example: The plateau phase ensures that the contraction and relaxation of the heart muscle are coordinated, preventing tetanus (sustained contraction), which would be fatal in cardiac tissue.

Comparison: Cardiac vs. Skeletal Muscle Action Potentials

• Skeletal Muscle: Short action potential, rapid contraction, allows summation and tetanus.

• Cardiac Muscle: Long action potential with plateau, contraction occurs during the action potential, preventing summation and tetanus.

Additional info: The long refractory period in cardiac muscle ensures that each contraction is followed by relaxation, allowing the heart chambers to refill with blood.

Excitation-Contraction Coupling in Cardiac Muscle

Cardiac muscle contraction is triggered by an action potential that propagates along the sarcolemma and T-tubules, leading to Ca2+ influx and subsequent contraction.

• T-tubules: Present but smaller than in skeletal muscle due to smaller cell size.

• L-type Ca2+ Channels: Located in the T-tubule membrane; open in response to depolarization, allowing extracellular Ca2+ to enter.

• Calcium-Induced Calcium Release (CICR): Influx of Ca2+ binds to ryanodine receptors on the sarcoplasmic reticulum (SR), causing a large release of Ca2+ into the cytosol ("calcium sparks").

• Troponin Binding: Ca2+ binds to troponin, initiating cross-bridge cycling and contraction (similar to skeletal muscle).

• Relaxation: Ca2+ is removed from the cytosol by:

  • SERCA (SR Ca2+-ATPase): Pumps Ca2+ back into the SR (primary active transport).

  • Na+/Ca2+ Exchanger (NCX): Exports Ca2+ in exchange for Na+ (secondary active transport).

  • Na+/K+ ATPase: Maintains Na+ gradient required for NCX function.

Additional info: Cardiac muscle contraction is striated and relies on the sliding filament mechanism, similar to skeletal muscle, but with unique regulatory features due to the role of extracellular Ca2+.

Cardiac Conduction System

Autorhythmic Cells and Pacemaker Activity

The heart contains specialized autorhythmic cells that generate spontaneous action potentials, setting the rhythm of the heartbeat.

• Locations: Sinoatrial (SA) node, Atrioventricular (AV) node, Purkinje fibers.

• Pacemaker Potential: Unlike other cells, these do not have a stable resting potential. Instead, they exhibit a slow depolarization (pacemaker potential) due to "funny" (If) channels that allow Na+ influx at hyperpolarized potentials (~ -60 mV).

• Depolarization: Once threshold is reached, voltage-gated Ca2+ channels open, causing rapid depolarization.

• Repolarization: K+ channels open, returning the cell to the trough, after which the cycle repeats.

Example: The SA node typically sets the pace at ~70 beats per minute. If the SA node fails, the AV node (~50 bpm) or Purkinje fibers (~30 bpm) can take over, though at slower rates.

Pathway of Electrical Conduction

• SA Node: Located in the right atrium; initiates the heartbeat and sets the pace.

• Internodal Pathways: Conduct impulses rapidly from the SA node to the AV node.

• Atrial Contraction: Impulse spreads through atrial muscle, causing atrial systole.

• AV Node: Delays the impulse to allow complete atrial contraction before ventricular contraction.

• AV Bundle (Bundle of His): Conducts the impulse from the AV node down the interventricular septum to the apex of the heart.

• Purkinje Fibers: Distribute the impulse throughout the ventricles, causing ventricular systole (contraction from apex upward).

Electrocardiogram (ECG/EKG) Interpretation

ECG Waves and Their Significance

An ECG records the electrical activity of the heart and is used to assess heart rate, rhythm, and conduction abnormalities.

Additional info: The QRS complex is larger than the P wave due to the greater muscle mass of the ventricles.

Common ECG Pathologies

Regulation of Heart Rate and Stroke Volume

Cardiac Output

Cardiac output (CO) is the volume of blood pumped by the heart per minute. It is determined by heart rate (HR) and stroke volume (SV).

• Formula:

• Typical Values: At rest, CO ≈ 5 L/min.

Autonomic Regulation of Heart Rate

• Parasympathetic (Vagus Nerve): Releases acetylcholine, increases K+ permeability, hyperpolarizes pacemaker cells, slows HR.

• Sympathetic: Releases norepinephrine/epinephrine, increases Na+ and Ca2+ permeability, depolarizes pacemaker cells, increases HR.

Additional info: Changes in ion permeability alter the slope of the pacemaker potential, affecting how quickly threshold is reached and thus the heart rate.

Regulation of Stroke Volume

• Intrinsic Control (Frank-Starling Law): Increased venous return stretches ventricular muscle, increasing force of contraction and stroke volume.

• Venous Tone: Increased venous constriction ("venous tone") returns blood to the heart more rapidly, increasing end-diastolic volume (EDV).

• Sympathetic Stimulation: Increases contractility by enhancing Ca2+ entry and cross-bridge formation, further increasing stroke volume.

Frank-Starling Mechanism: The greater the stretch of the ventricular muscle (within physiological limits), the greater the force of contraction.

Summary Table: Cardiac Muscle vs. Skeletal Muscle

Key Terms

• Cardiac Output (CO): Volume of blood pumped per minute.

• Stroke Volume (SV): Volume of blood pumped per beat.

• Heart Rate (HR): Number of beats per minute.

• Autorhythmic Cells: Specialized cardiac cells that generate spontaneous action potentials.

• Frank-Starling Law: The relationship between EDV and stroke volume.

• ECG/EKG: Electrocardiogram, a recording of the heart's electrical activity.

• Sinus Tachycardia/Bradycardia: Abnormally fast/slow heart rate originating from the SA node.

• Atrial Fibrillation: Uncoordinated atrial contraction.

• AV Block: Impaired conduction between atria and ventricles.

• Sinus Arrest: Failure of the SA node to initiate an impulse.